Four Hypotheses are proposed for investigation. Hypothesis 1. The kidneys from gravid rats have increased expression of NO synthase (NOS), which contributes to the NO-dependent renal vasodilation and hyperfiltration of pregnancy. Hypothesis 2. Increased activation of the endothelin (RES-701-1 antagonist sensitive) B receptor subtype located on the endothelium contributes to NO-dependent renal vasodilation and hyperfiltration in gravid rats. Hypothesis 3. Relaxin also contributes to NO-dependent renal vasodilation and hyperfiltration in gravid rats. Hypothesis 4. Relaxin contributes to renal vasodilation, hyperfiltration, and osmoregulatory changes in gravid women.